The Impact of Maternal Obesity on Offspring Obesity via Programmed Adipogenesis and Appetite

Abstract

Obesity and its related diseases are the leading causes of death in Western society. In concert with the epidemic of obesity among children and adults, there has been a marked and continuing increase in the prevalence of obesity and accompanying gestational diabetes among women presenting for prenatal care. Results from both human and animal studies indicate that in utero environment may contribute importantly to the developmental programming of adult obesity. Remarkably, considering cellular divisions necessary for organ and body growth (not including cell turnover), over 90% of lifetime cell divisions occur by the time of birth. Thus, it should not be surprising that the maternal/fetal environment may alter cell signaling, epigenetic regulation, and organ development. As energy and nutrition balance are the ultimate endpoints of organ systems regulating energy balance, it would be further expected that the fetal nutrient environment may impact systems regulating food intake and energy storage. In this chapter, we present evidence of the effects of maternal obesity, gestational diabetes, and high-fat Western diets on the development of the hypothalamic appetite network and adipose tissue. Through the interplay of extracellular signaling factors, intracellular transcription responses, and nutrient-induced epigenetic alterations, the maternal environment can program fetal/newborn energy pathways resulting in a predisposition toward obesity. This predisposition is especially paramount within a postnatal environment that facilitates neonatal growth as well as access to energy-intense childhood and adult diets. These findings have great significance for prenatal, neonatal, and childhood care.